RSA Modulation as a Cardiovascular-Relevant Pathway of Adversity

Cardiovascular disease remains the leading cause of mortality worldwide, yet the developmental origins of cardiovascular vulnerability are not fully understood. A growing body of research indicates that early environmental adversity is associated with increased risk for adverse mental and physical outcomes, including cardiovascular disease. However, the psychophysiological mechanisms linking early adversity to long-term cardiovascular health remain unclear. One promising pathway involves autonomic nervous system regulation, particularly the flexible control of the heart rate via the parasympathetic nervous system. This study investigates respiratory sinus arrhythmia (RSA) modulation as a index of vagal flexibility, reflecting the parasympathetic nervous system's capacity to adaptively regulate cardiac function in response to changing environmental and physiological demands. RSA represents the inhibitory influence of the vagus nerve on the heart , and effective modulation from rest to physical challenge is thought to reflect efficient autonomic modulation. Reduced RSA modulation from baseline to exercise may indicate diminished vagal flexibility, which has been linked to stress-related psychopathology and increased cardiovascular risk. Rather than conceptualizing adversity as a cumulative score, this study adopts a dimensional approach to childhood adversity, distinguishing between threat related experiences (e.g. exposure to violence or harm) and deprivation related experiences (e.g. absence of expected cognitive or material inputs). This approach allows for more precise examination of how distinct forms of adversity may differentially impact physiological regulation. The primary aim of this study is to examine the age related changes in RSA modulation from resting baseline to moderate exercise across development, spanning early adolescence through mid-adulthood (ages 12-40). RSA will be assessed during a resting baseline and during two exercise conditions (handgrip squeezing and elliptical pedaling), allowing for quantification of RSA change across physiological states. It is hypothesized that the magnitude of RSA modulation will decrease with increasing age. A secondary aim is to examine whether threat and deprivation are differentially associated with RSA modulation. It is hypothesized that greater exposure to threat, but not deprivation, will be associated with smaller RSA changes from baseline to exercise. A final aim is to test whether threat interacts with age, such that age related reductions in RSA modulation are accelerated among individuals exposed to higher levels of threat, whereas deprivation is not expected to show this interaction. By integrating developmental psychophysiology with a dimensional model of childhood adversity, this project aims to clarify how early environmental experiences become biologically embedded in autonomic systems relevant to long-term cardiovascular health. Understanding these mechanisms may inform early identification of cardiovascular vulnerability and contribute to prevention focused models of health across the lifespan.